The neonate arrived at our institution in extremis
(heart rate, 59 beats/min; mean arterial pressure, 50 mmHg; SpO2
, 62%). Venoarterial extracorporeal membrane oxygenation was initiated via
the right internal jugular vein and the right internal carotid artery. Computed tomography showed absent lung aeration, the arterial cannula (fig. 1A
, ac), subcutaneous emphysema (fig. 1A
, white arrows), and the endotracheal tube diverging from the midline (fig. 1A
, black arrows). Bronchoscopy by the otorhinolaryngologist confirmed a laryngeal tear with a ruptured anterior commissure (fig. 1B
, asterisks) through which the endotracheal tube traveled into the mediastinum. The otorhinolaryngologist repositioned the endotracheal tube into the native trachea (fig. 1B
). Support was withdrawn 6 days later after progression of hypoxic ischemic injury. Autopsy findings included a hypoplastic thyroid cartilage that likely resulted in an inherent weakness of the anterior tracheal wall.
Traumatic delivery and endotracheal intubation can cause life-threatening tracheal and laryngeal injuries in neonates.1
Development of cervical emphysema before intubation suggests that this child’s laryngeal rupture was caused by a difficult delivery rather than traumatic intubation. Fiberoptic endoscopy should be used to investigate potential airway rupture, with emergent otorhinolaryngology consultation and deferral of endotracheal intubation until direct airway visualization has been accomplished.2
Extracorporeal membrane oxygenation should be considered early if direct airway visualization cannot be performed.3
The authors declare no competing interests.